Outline

Objective: Delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage (SAH) leading to delayed ischemic neurological deficits, may be evoked by a disturbance in vasomotor equilibrium, to which two major physiologically antagonistic compounds nitric oxide (NO) and ET-1 may contribute. Increased CSF levels of ADMA have been associated with the course and degree of cerebral vasospasm in a primate model and in patients after SAH. We sought to determine, if alterations of ADMA and ET-1 levels are associated with cerebral vasospasm and/or ischemic lesions after SAH.

Methods: Levels of ADMA and ET-1 were determined in CSF from 35 patients after SAH. Cerebral arteriograms were performed to detect vasospasm and CT-scans to verify ischemic brain lesions. Results: CSF ADMA levels were correlated with the development of vasospasm (p<0.01) and increased only in patients with vasospasm (p<0.01). ET-1 CSF levels remained unchanged in patients with and without vasospasm.

Results: CSF ADMA levels were correlated with the development of vasospasm (p<0.01) and increased only in patients with vasospasm (p<0.01). ET-1 CSF levels remained unchanged in patients with and without vasospasm.

Conclusions: Levels of CSF ADMA, but not ET-1, significantly correlate with development of vasospasm after SAH. ADMA and ET-1 were not correlated with ischemia verified on follow-up CCT scans. ADMA via NO, seems to be involved in the development of cerebral vasospasm after SAH, causing an imbalance of vasodilative and vasoconstrictive components, whereas ET-1 may sustain and/or enforce this imbalance.